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Disruptions in lipid homeostasis have been observed in many neurodevelopmental disorders that are associated with dendrite morphogenesis defects. However, the molecular mechanisms of how lipid homeostasis affects dendrite morphogenesis are unclear. We find that easily shocked (eas), which encodes a kinase with a critical role in phospholipid phosphatidylethanolamine (PE) synthesis, and two other enzymes in this synthesis pathway are required cell autonomously in sensory neurons for dendrite growth and stability. Furthermore, we show that the level of Sterol Regulatory Element-Binding Protein (SREBP) activity is important for dendrite development. SREBP activity increases in eas mutants, and decreasing the level of SREBP and its transcriptional targets in eas mutants largely suppresses the dendrite growth defects. Furthermore, reducing Ca2+ influx in neurons of eas mutants ameliorates the dendrite morphogenesis defects. Our study uncovers a role for EAS kinase and reveals the in vivo function of phospholipid homeostasis in dendrite morphogenesis. Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.

Citation

Shan Meltzer, Joshua A Bagley, Gerardo Lopez Perez, Caitlin E O'Brien, Laura DeVault, Yanmeng Guo, Lily Yeh Jan, Yuh-Nung Jan. Phospholipid Homeostasis Regulates Dendrite Morphogenesis in Drosophila Sensory Neurons. Cell reports. 2017 Oct 24;21(4):859-866


PMID: 29069593

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